Boulloche J, Mallet E, de Menibus C H
Arch Fr Pediatr. 1987 Feb;44(2):85-9.
A historical cohort study was undertaken to determine the risk of epilepsy in a population of 18 newborns with neonatal hypoglycemia due to insulin excess. Follow-up was 3 years 8 months (range 7 years-1 year 3 months). Insulin excess was associated with maternal diabetes in 13 infants, with an isolated macrosomia in 2 infants, in one case with probable Langerhans hyperplasia, and in 2 newborns only prolonged beta-sympathomimetic therapy was the possible cause of insulin excess. Newborns with anoxia, brain malformation or small for date were excluded. Two newborns had hypoglycemia with epileptic clonic seizures, but only one was later epileptic. In this case, hypoglycemia was severe and persistent (16 hours). Hyperinsulinism was related to Langerhans hyperplasia. CT scan made at ages one and 6 months showed large hypodensity of the frontal and occipital white matter. Visual evoked responses were also abnormal. Visual evoked responses and CT scan normalized at 1 year. In other children, asymptomatic hypoglycemia (n = 11) or symptomatic hypoglycemia without epileptic seizures (n = 5) did not increase the epileptic risk as none of them had epileptic seizure later on. Thus, seizures associated with neonatal hypoglycemia alone seem to increase the epileptic risk with duration and severity of hypoglycemia being also essential prognostic factors.
开展了一项历史性队列研究，以确定18名因胰岛素过量导致新生儿低血糖的人群中癫痫的风险。随访时间为3年8个月（范围为7年至1年3个月）。13名婴儿的胰岛素过量与母亲糖尿病有关，2名婴儿与单纯巨大儿有关，1例可能与朗格汉斯细胞增生有关，2名新生儿仅长期使用β-拟交感神经药治疗可能是胰岛素过量的原因。排除有缺氧、脑畸形或小于胎龄儿的新生儿。2名新生儿出现低血糖伴癫痫阵挛发作，但只有1名后来患癫痫。在这种情况下，低血糖严重且持续（16小时）。高胰岛素血症与朗格汉斯细胞增生有关。1岁和6个月时进行的CT扫描显示额叶和枕叶白质大片低密度。视觉诱发电位也异常。视觉诱发电位和CT扫描在1岁时恢复正常。在其他儿童中，无症状低血糖（n = 11）或有症状但无癫痫发作的低血糖（n = 5）并未增加癫痫风险，因为他们后来都没有癫痫发作。因此，仅与新生儿低血糖相关的癫痫发作似乎会增加癫痫风险，低血糖的持续时间和严重程度也是重要的预后因素。
